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Featured researches published by C. Trautwein.


Clinical and Experimental Immunology | 2008

Clonal analysis of liver-infiltrating T cells in patients with LKM-1 antibody-positive autoimmune chronic active hepatitis

H Löhr; M. Manns; A. Kyriatsoulis; A.W. Lohse; C. Trautwein; K.-H. Meyer zum Büschenfelde; B. Fleischer

Autoantibodies against microsomal antigen of liver and kidney (LKM‐1) are diagnostic markers for a subgroup of autoimmune chronic active hepatitis (AI‐CAH). Cytochrome P4S0dbl, now classified as cytochrome P450 IID6, is the major antigen of LKM‐1 antibodies. Immunohistological studies suggest that hepatic injury in AI‐CAH is mediated by liver‐infiltrating T cells. In the present study the specificity and function of liver‐infiltrating T cells was analysed at the clonal level. Phenotypical characterization of 189 T cell clones isolated from four liver biopsies of LKM‐1 antibody‐positive patients showed an enrichment of CD4+CD8‐ T cells. Five CD4+CD8‐ T cell clones proliferated specifically in the presence of recombinant human LKM‐1 antigen (rLKM). This reaction was restricted to autologous antigen‐presenting cells and to HLA class II molecules. In order to see whether rLKM was also recognized by peripheral blood T lymphocytes (PBL) we tested the proliferative response of PBL from several individuals. PBL from three of the four patients with LKM‐1 antibody‐positive AI‐CAH proliferated to rLKM, whereas no response was seen with PBL from patients with LKM‐1 antibody‐negative chronic liver diseases and from healthy blood donors. These data demonstrate that the LKM‐1 antigen is recognized by liver‐infiltrating T cells in LKM‐1 antibody‐positive AI‐CAH. For further functional characterization, liver‐derived T cell clones were tested for their cytotoxic activity. In the presence of phytohacmagglutinin 24 out of 26 CD4‐CD8+ but also 20 out of 63 CD4+CD8‐ T cell clones lysed autologous as well as allogenic EBV‐transformed B cell lines or K562 cells. Five CD4‐CD8+ T cell clones lysed autologous but not allogenic B cell lines spontaneously in a HLA class I‐restricted manner. Although the antigen specificity of these clones is still unknown the data show the presence of autoreactive T cells at the site of inflammation that could contribute in the pathogenesis of AI‐CAH.


Journal of Biological Chemistry | 1999

The designer cytokine hyper-interleukin-6 is a potent activator of STAT3-dependent gene transcription in vivo and in vitro.

Tim Rakemann; Monika Niehof; Stefan Kubicka; Martina Fischer; Michael Manns; Stefan Rose-John; C. Trautwein

Interleukin-6 (IL-6) triggers pivotal pathwaysin vivo. The designer protein hyper-IL-6 (H-IL-6) fuses the soluble IL-6 receptor (sIL-6R) through an intermediate linker with IL-6. The intracellular pathways that are triggered by H-IL-6 are not defined yet. Therefore, we studied the molecular mechanisms leading to H-IL-6-dependent gene activation. H-IL-6 stimulates haptoglobin mRNA expression in HepG2 cells, which is transcriptionally mediated as assessed by run-off experiments. The increase in haptoglobin gene transcription correlates with higher nuclear translocation of tyrosine-phosphorylated STAT3 and its DNA binding. As H-IL-6 stimulates STAT3-dependent gene transcription, we compared the molecular mechanism between IL-6 and H-IL-6. Transfection experiments were performed with a STAT3-dependent luciferase construct. The same amount of H-IL-6 stimulated luciferase activity faster, stronger, and for a longer period of time. Dose response experiments showed that a 10-fold lower dose of H-IL-6 stimulated STAT3-dependent gene transcription comparable with the higher amount of IL-6. Cotransfection with the gp80 and/or gp130 receptor revealed that the effect of H-IL-6 on STAT3-dependent gene transcription is restricted to the gp80/gp130 receptor ratio. High amounts of gp130 increased and high amounts of gp80 decreased the effect on H-IL-6-dependent gene transcription. To investigate the in vivo effect of H-IL-6 on gene transcription in the liver, H-IL-6 and IL-6 were injected into C3H mice. H-IL-6 was at least 10-fold more effective in stimulating the DNA binding and nuclear translocation of STAT3, which enhances haptoglobin mRNA and protein expression. Thus H-IL-6 stimulates STAT3-dependent gene transcription in liver cells in vitro and in vivo at least 10-fold more effectively than IL-6. Our results provide evidence that H-IL-6 is a promising designer protein for therapeutic intervention during different pathophysiological conditions also in humans.


Biochemical and Biophysical Research Communications | 1992

Regulation of cytochrome P450 IID by acute phase mediators in C3HHeJ mice

C. Trautwein; G. Ramadori; Guido Gerken; K.-H. Meyer zum Büschenfelde; M. Manns

Cytochrome P450 IID6 is a drug metabolizing enzyme and the major target antigen in LKM-1 antibody positive chronic active hepatitis. The histological hallmark of chronic active hepatitis is a lymphocytic infiltrate in the liver. It is unknown whether and how cytokines produced and secreted by these tissue infiltrating mononuclear cells regulate the cellular expression of cytochrome P450 IID6. To study the effect of interleukin 1, tumor necrosis factor and interleukin 6 on the hepatocellular RNA expression of cytochrome P450 IID, we injected each of the cytokines in C3H/HeJ mice. We found a time-dependent suppression of the cytochrome in the liver. Six hours after the intraperitoneal injection of 0.5 micrograms interleukin 1 beta the specific RNA-expression was reduced to 25% of the original level. A similar reduction was found after the injection of 2 micrograms tumor necrosis factor alpha. A mild suppression to 65% of the original level was seen six hours following the dose of 100 ng interleukin 6. Our studies show how immune mediators can change the expression of an autoantigen. Further studies in the human system are necessary to estimate this regulation for the elimination of drugs and in LKM-1 antibody positive chronic active hepatitis.


Annals of the Rheumatic Diseases | 1991

Candida arthritis: cellular immune responses of synovial fluid and peripheral blood lymphocytes to Candida albicans.

E. Hermann; Werner-Johannes Mayet; O. Klein; A.W. Lohse; C. Trautwein; I Michiels; T. Poralla; K H Meyer zum Büschenfelde

A case of septic Candida albicans arthritis of the knee in a patient with systemic candidiasis is presented. Systemic and intra-articular cellular immune responses to C albicans and various bacterial antigens were monitored for 15 weeks. It is shown that the candida induced blastogenesis of synovial fluid lymphocytes was much more stimulated than that of peripheral blood lymphocytes, and that the proportion of activated cells expressing HLA class II antigens was markedly increased in the synovial fluid. Strong cellular immune responses to Candida albicans could still be shown many weeks after the synovial fluid aspirates had become sterile. For the first time synovial fluid derived, CD4 positive T lymphocyte clones with specificity for candida antigens were characterised and further propagated in vitro.


Bildverarbeitung für die Medizin | 2011

Segmentierung von Blutgefäßstrukturen in koloskopischen NBI-Bilddaten

Sebastian Gross; Stephan Palm; Alexander Behrens; Jens J. W. Tischendorf; C. Trautwein; Til Aach

Bei der arztlichen Einschatzung von Dickdarmpolypen kommt das neue Verfahren Narrow Band Imaging zum Einsatz. Hierbei wird der Kontrast der charakteristischen Blutgefase durch Modifikation der Beleuchtung deutlich angehoben, wodurch diese dann als Entscheidungsgrundlage herangezogen werden konnen. Aufbauend auf diesem Verfahren ist eine automatische Segmentierung der Blutgefase und Klassifikation der Dickdarmpolypen moglich. In diesem Paper werden Verbesserungen fur die Blutgefassegmentierung des von Stehle et al. vorgeschlagenen Verfahrens erlautert und Ergebnisse im Vergleich dargestellt. Es zeigt sich, dass sowohl die Qualitat der Segmentierung als auch die Ergebnisse der automatisierten Klassifikation deutlich gesteigert werden konnten.


Journal of Hepatology | 2004

55 Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of lamivudine-resistant mutants

Frank Tacke; C. Gehrke; Albert Heim; Michael P. Manns; C. Trautwein

During chronic hepatitis B virus (HBV) infection, mutations in the precore (PC) or basal core promoter (BCP) region affecting HBV e antigen (HBeAg) expression occur commonly and represent the predominant virus species in patients with HBeAg-negative chronic hepatitis B. The PC mutation (G1896A+C1858T) creates a translational stop codon resulting in absent HBeAg expression, whereas BCP mutations (A1762T/G1764A) reduce HBeAg expression by transcriptional mechanisms. Treatment of chronic HBV infection with lamivudine (LMV) often selects drug-resistant strains with single (rtM204I) or double (rtL180M+rtM204V) point mutations in the YMDD motif of HBV reverse transcriptase. We cloned replication-competent HBV vectors (genotype A, adw2) combining mutations in the core (wild type [wt], PC, and BCP) and polymerase gene (wt, rtM204I, and rtL180M/M204V) and analyzed virus replication and drug sensitivity in vitro. Resistance to LMV (rtM204I/rtL180M+rtM204V) was accompanied by a reduced replication efficacy as evidenced by reduced pregenomic RNA, encapsidated progeny DNA, polymerase activity, and virion release. PC mutations alone did not alter virus replication but restored replication efficacy of the LMV-resistant mutants without affecting drug resistance. BCP mutants had higher replication capacities than did the wt, also in combination with LMV resistance mutations. All nine HBV constructs showed similar sensitivities to adefovir. In conclusion, BCP-PC mutations directly impact the replication capacity of LMV-resistant mutants. PC mutations compensated for replication inefficiency of LMV-resistant mutants, whereas BCP mutations increased viral replication levels to above the wt baseline values, even in LMV-resistant mutants, without affecting drug sensitivity in vitro. Adefovir may be an effective treatment when combinations of core and polymerase mutations occur.


Hepatology | 1987

Two different subtypes of antimitochondrial antibodies are associated with primary biliary cirrhosis: Identification and characterization by radioimmunoassay and immunoblotting

Michael Manns; Guido Gerken; A. Kyriatsoulis; C. Trautwein; Konrad Reske; Karl-Hermann Meyer zum Büschenfelde


Archive | 2005

Viral variants and uses therefor

Thomas Bock; Hans L. Tillmann; Michael Manns; C. Trautwein; Stephen Locarnini; Joseph Torresi


/data/revues/00165107/v63i5/S0016510706006778/ | 2011

Characterization of Dominant Bile Duct Stenoses in Patients with Primary Sclerosing Cholangitis Using Cholangioscopy

Jens J. W. Tischendorf; Martin Krueger; C. Trautwein; Nina Duckstein; Andrea S. Schneider; Michael Manns; Peter N. Meier


Journal of Hepatology | 2004

199 Impaired pulmonary function in liver cirrhosis is a relevant factor for elevated erythropoietin levels in patients with chronic liver disease

Frank Tacke; Patrick Schöffski; Arnold Ganser; Michael P. Manns; C. Trautwein

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Frank Tacke

RWTH Aachen University

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